The Puzzle of Vitiligo, Oxidative Stress and Narrow Band Ultraviolet-B

Obviously, vitiligo is a multifactorial disease, and at this stage, we all accept that the autoimmune theory, the adhesion defect theory and the biochemical theory based on oxidative stress are the mainstays of our current knowledge about the aetiology of the disease. The presence of an imbalance in the anti-oxidant system in vitiligo melanocytes was assessed early, providing support for a free radical-mediated damage as an initial pathogenic event in melanocyte degeneration in vitiligo [1,2]. Since then, it was demonstrated that vitiligo patients had an increased epidermal level of H2O2 but also an increased superoxide dismutase (SOD) activity, especially in active lesions [3,4]. Not surprisingly, systemic antioxidants provide a helpful adjuvant in the treatment of vitiligo, as well as topical antioxidants, among them combinations of SOD and catalase (CAT) whose activity has been reported as similar to that of 0.05% betamethasone [5].